Ventricular pacing has been a useful technique for at least 50 years, and transvenous pacing for nearly that long. In the transvenous pacing system the lead is placed from a vein, usually in the thorax, and threaded into the right ventricle 22 of the heart 10. The lead in the right ventricle 22 permits pacing and sensing within that chamber. Of course, pacing from the right ventricle 22 depolarizes the heart in a completely different way than the heart is normally depolarized and does not make use of the patient's own, usually diseased, conduction system. The indication for pacing is an impairment of the patient's conduction system which prevents the system from being able to transmit electrical impulses that allow the heart to depolarize. The depolarization process is what leads to contraction in the cardiac muscle and a beat of the heart. Ventricular pacing, however, while very effective in preventing deaths from such entities as complete heart block, has several problems associated with it. One problem associated with ventricular pacing is pacemaker syndrome, which is a hemodynamic abnormality that can result when use of ventricular pacing is, for example, uncoupled from the atrial contraction. It can also result from a less effective contraction caused by the abnormal mechanism of depolarization caused by the right ventricular pacing catheter. In other words, the heart, depolarized from the right ventricular apex, does not squeeze as efficiently as the heart would have squeezed if it had been depolarized by its own conduction mechanism. Patients sense the decline in cardiac output when their pacemaker kicks in. In other patients, pacing induces a long term malfunction of the heart called cardiomyopathy that is caused by this slower depolarization of the heart and the associated decline in pump efficiency.
Over the past five to six years, first Medtronic and then other companies have developed devices to counter the deleterious effects of ordinary right ventricular apex pacing. The basic idea is to use two different pacing catheters in different parts of the ventricles 22, 26 to simultaneously depolarize the heart. This is called biventricular (or biV) pacing. Biventricular pacing (also referred to as cardiac resynchronization therapy (CRT)) uses leads that stimulate the right ventricle 22 from the apex and the left ventricle 26 from the lateral wall via the coronary sinus. One of the electrodes is the standard right ventricular apical pacing catheter and the other is a left ventricular lead usually placed, as indicated above, on the posterior left ventricular wall 15 through a vein branch 6 of the coronary sinus 5. When these two leads are hooked together to the same generator and simultaneously stimulate the ventricle, it takes less time to depolarize the ventricle and therefore a more synchronous contraction of the muscle ensues. The heart pumps blood more efficiently.
Biventricular pacing is also indicated for patients with congestive heart failure (CHF) due to left ventricular dysfunction. It is estimated that in approximately 30% of patients with heart failure, an abnormality in the heart's electrical conducting system causes the heart to beat in an asynchronous fashion. That is, the left ventricle fails to contract toward its theoretical center of mass. This asynchrony greatly reduces the efficiency of the heart in some patients with heart failure. Biventricular pacing resynchronizes the contraction of the heart by shortening the actuation time of the ventricles. Biventricular pacemakers differ from other pacemakers, which pace only the right ventricle 22. Biventricular pacing systems (BVPS), as they are currently constituted, require an operator to thread a catheter from an introducer in the coronary sinus 80 down into a vein branch 82 of the coronary sinus 80, shown in FIG. 1C, and then wedge that lead into the branch 82 to hold it in position. This technique has been useful but has had some difficulty associated with it and therefore a supplanting technique to solve such difficulty is desirable. Additionally, one of the risks associated with placement of the device is the potential to damage the coronary sinus or coronary veins by, e.g., dissection or perforation.
Biventricular pacing has now demonstrated utility in several situations. For example, it reverses the symptoms in patients with the pacemaker syndrome described above. It also improves many cardiomyopathies caused by long term pacing. In addition, it improves cardiac contraction in some patients who have enlarged ventricles 22, 26 and prolonged QRS duration who are suffering from heart failure. It has been sufficiently useful so that it is now included in many of the latest models of internal cardioverters and defibrillators (ICD) which are used to treat patients with heart failure and arrhythmia. See, for example, InSync Sentry™ and InSync Maximo™ (www.medtronic.com). Biventricular pacing is now a standard part of the armamentarium and medical science accepts that biventricular pacing, because it leads to more synchronous contraction, is a better way to pace patients than pacing from the right ventricular apex alone. A conventional implantable medical device, such as an ICD, is coupled to a patient's heart by leads such that the patient's heart forms part of the circuit. The device may include, for example, a pacemaker or defibrillator or any device that performs pacing or defibrillating functions. A housing houses a battery and pacing or defibrillating circuitry. Each lead typically is adapted to engage at least one stimulating electrode for delivery of electrical impulses to excitable myocardial tissue. The leads can be unipolar or bipolar.
Notwithstanding the clinical benefits of biventricular pacing, correctly placing the LV lead to achieve optimum performance may be difficult. The placement of the first lead, the one that goes in the right ventricle 22, has been standard for fifty years. When biventricular pacing was first tried, the placement of the second left ventricular lead was done surgically. However, the surgical procedure requires a small incision in the chest and most cardiologists cannot do this and do not want to refer patients to surgeons. Therefore, the standard cardiologic technique for LV lead placement now requires placement of a sheath from the subclavian vein into the coronary sinus 80 and through that sheath, an angiogram of the coronary sinus 80 can be obtained. From the angiogram the branches 82 of the coronary sinus 80 can be identified and a small pacing catheter is then directed through the coronary sinus and into the small coronary sinus vein 82 (see FIG. 1C) where it is lodged. The guiding catheter is then removed and the patient has a lead on the posterior left ventricular wall 15 (see FIG. 1C). The exact location of the lead is therefore a prisoner of the accidental anatomy of the veins that feed into the coronary sinus 5. The optimal location of the left ventricular lead and solutions for routine pacing from this location have not previously been discussed.